This project has four major objectives; 1)to elucidate the nonvisual molecular function of vitamin A, 2)to isolate and characterize cellular receptors for vitamin A, 3)to develop better procedures for evaluating the vitamin A status of experimental animals and humans, and 4)to determine the factors leading to increased susceptibility to infection in vitamin A deficiency. With respect to the nonvisual function of vitamin A we will investigate 1)the relative role(s) of vitamin A in the differentiation and biosynthetic function of goblet cells, 2)the metabolic interrelationships between altered RNA, amino acid and intermediary metabolism in acute vitamin A deficiency, 3)the role of vitamin A in ascorbate synthesis and 4)the metabolism and possible physiological effects of taurine in vitamin A deficiency. With respect to cellular receptors for vitamin A, we will characterize subcellular fractions that are preferentially labeled following the injection of 1)labeled retinol, and 2)labeled retinol-RBP complex. These receptors will be compared with those obtained after the incubation of cell homogenates with labeled retinol. The binding of labeled gamma-retinol and 3, 5 epoxy retinol will be used to check the specificity of binding of both classes of receptors. With respect to whole body vitamin A status, we aim to refine a novel isotope exchange method enabling the preparation of deuterated derivatives of vitamin A. Finally, to assess the role of vitamin A in the immune responses of the body we will study lymphoid tissue morphology, cell mediated immunity, and the quantity and quality (Ko) of systemic and secretory antibodies in vitamin A deficiency. The functional integrity of the local immune response will also be evaluated.